CLINICAL-PATTERN AND CLINICAL NEUROPHYSIO LOGY OF SPASTICITY .2. CLINICAL-PATTERN AND CLINICAL NEUROPHYSIOLOGY

Authors
Citation
J. Noth, CLINICAL-PATTERN AND CLINICAL NEUROPHYSIO LOGY OF SPASTICITY .2. CLINICAL-PATTERN AND CLINICAL NEUROPHYSIOLOGY, Aktuelle Neurologie, 24(5), 1997, pp. 188-193
Citations number
56
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
ISSN journal
03024350
Volume
24
Issue
5
Year of publication
1997
Pages
188 - 193
Database
ISI
SICI code
0302-4350(1997)24:5<188:CACNLO>2.0.ZU;2-V
Abstract
Spasticity develops in response to both acute and chronic lesions of d escending motor pathways of the CNS. Spinal and supraspinal lesions of various aetiology, including stroke, can cause spasticity. Spasticity is thus one of the most frequent syndromes in neurology. Spasticity i s characterised by a velocity-dependent increase in tonic stretch refl exes. Spastic muscle tone can easily be distinguished from other forms of increased muscle tone by its elastic nature and the presence of as sociated symptoms, such as exaggerated tendon and cutaneous reflexes, clonus, Babinski's sign and autonomic hyperreflexia; In most cases, sp asticity is preceded by a period of flaccid paresis of the affected mu scles, the duration of which may sometimes be prolonged. Conditions th at favour the persistence of these flaccid pareses are: advanced age, a very extended lesion, sensorimotor neglect-and involvement of the le ntiform nucleus within the lesion. On the other hand, conditions for a favourable recovery of motor function subsequent to flaccid paresis a re: intactness of the basal ganglia, or of the lateral thalamus. Patie nts with isolated lesions of the anterior or posterior limb of the int ernal capsule also have a favourable functional outcome, since the int actness of parts of the corticospinal tract seems to be a prerequisite for good functional recovery. The spastic muscle tone, tested by the clinician by means of fast passive stretchings, is caused by enhanced excitability of alpha motoneurons, However, if the patient voluntarily moves the spastic limb, i.e. during walking, the stretch-induced acti vity cannot be detected in the antagonists. Thus, other factors are re sponsible for the slowing-down of the self-paced voluntary movement in patients suffering from spasticity, such as paresis of the agonist an d transformations of muscle fibres of spastic muscles. These transform ations may lead to increased stretch resistance of spastic muscle fibr es (stretch activation).